ArticleMolecular oral microbiology2018
Deficiency of BrpA in Streptococcus mutans reduces virulence in rat caries model.
Article in Molecular oral microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
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- Structural Determination of Glucosyltransferase C by Cryo-Electron Microscopy.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Growth with Commensal Streptococci AltersJournal of dental research · 2023Article
- [Research Updates: Cariogenic Mechanism ofSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022Review
- Strategies for dispersion of cariogenic biofilms: applications and mechanisms.Frontiers in microbiology · 2022Review
- Anti-Biofilm Activity of Cannabigerol againstMicroorganisms · 2021Article
- Effects of Rhein-8-O-β-D-glucopyranoside on the Biofilm Formation of Streptococcus mutans.Current microbiology · 2021Article
- CRISPR-Pathogens (Basel, Switzerland) · 2020Article
- The Impacts of Sortase A and the 4'-Phosphopantetheinyl Transferase Homolog Sfp onFrontiers in microbiology · 2020Article
- Insight into the Effect of Small RNAIndian journal of microbiology · 2019Article
- Structural Characterization of theMolecules (Basel, Switzerland) · 2018Article
- Deficiency of MecA inFrontiers in microbiology · 2018Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Our recent studies have shown that BrpA in Streptococcus mutans plays a critical role in cell envelope biogenesis, stress responses, and biofilm formation. In this study, a 10-species consortium was used to assess how BrpA deficiency influences the establishment, persistence, and competitiveness of S. mutans during growth in a community under conditions typical of the oral cavity. Results showed that, like the wild-type, the brpA mutant was able to colonize and establish on the surfaces tested. Relative to the wild-type, however, the brpA mutant had a reduced ability to persist and grow in the 10-species consortium (P < .001). A rat caries model was also used to examine the effect of BrpA, as well as Psr, a BrpA paralog, on S. mutans cariogenicity. The results showed no major differences in infectivity between the wild-type and the brpA and psr mutants. Unlike the wild-type, however, infection with the brpA mutant, but not the psr mutant, showed no significant differences in both total numbers of carious lesions and caries severity, compared with the control group that received bacterial growth medium (P > .05). Metagenomic and quantitative polymerase chain reaction analysis showed that S. mutans infection caused major alterations in the composition of the rats' plaque microbiota and that significantly less S. mutans was identified in the rats infected with the brpA mutant compared with those infected with the wild-type and the psr mutant. These results further suggest that BrpA plays a critical role in S. mutans pathophysiology and that BrpA has potential as a therapeutic target in the modulation of S. mutans virulence.
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